In the United States, stroke-related illness is the third leading cause of death. Each year approximately 400,000 individuals in this country suffer a stroke. For those who survive, it is a major cause of long-term disability. Of every 100 persons surviving an acute stroke, it is estimated that only 10 are able to return to-their previous activities without significant impairment. Forty percent of all individuals suffering an acute stroke episode are disabled to the extent that they require special assistance and, of these, ten percent need institutional care.
As will be appreciated by those skilled in the art, stroke is the interruption of normal blood flow in a region of the brain. This interruption of blood flow causes an oxygen deficit in the tissues of the brain which in turn produces unconsciousness and paralysis. Depending upon the severity of the oxygen deprivation, paralysis may be temporary or permanent. Stroke (or apoplexy) occurs most commonly as the result of a cerebral thromboembolism or cerebral hemorrhage and may also be caused by a cerebral embolism. Many strokes are linked to pre-existing conditions such as atherosclerosis, hypertension or an arterial aneurysm.
Cerebral function is primarily dependent upon an adequate supply of oxygen, glucose and other nutrients to the brain as provided by blood flow. In brain tissue, a high rate of glucose oxidation is necessary to meet the energy requirements of cellular ion pumps which maintain the sodium and potassium gradients across cell membranes. Because there is no significant storage of oxygen and glucose in cerebral tissue, neurons are dependent on adequate cerebral blood flow to deliver oxygen and glucose. When cerebral blood flow is interrupted, as in a stroke, tissue ischemia rapidly ensues. The neurons then become hypoxic. The effect of ischemia on the neuron is failure of the ion pumps which, as stated, are required to maintain ionic distribution across the membrane. There is a consequent rapid leakage of K.sup.+ ions from within the cell to the extracellular volume. Carrier-mediated uptake of C1.sup.- ions, resulting from elevated levels of K.sup.+ ions and stimulated by HCO.sub.3.sup.- ions, carries Na.sup.+ ions and water into astrocytes. This initiates a vicious cycle whereby astroglial edema is increased which exacerbates tissue ischemia. The increasingly ischemic neurons then leak more K.sup.+ ions into the extracellular space which further exacerbates the astroglial edema. The difficulties of post-stroke patient management are further complicated when blood flow is restored following a vascular accident due to a concomitant abrupt rise in water content in the tissue.
Various therapeutic measures have been used by others to treat the often fatal sequelae of stroke. In the final analysis, successful stroke therapy must be directed at preventing or minimizing the consequences of the initial acute circulatory failure and the resultant tissue ischemia. The target of such treatment is often the ischemic neuron or the cerebral ischemia edema that accompanies stroke. Glucocorticoid steroids, including dexamethasone and cortisone, have been administered in experimental trials, as well as agents that act as diuretics and/or inhibitors of anion transport. The latter have been useful in inhibiting the production of cerebrospinal fluid. Another therapeutic approach has been the use of barbiturates in anesthetic doses, which is presumed to relate to the associated depression of neuronal metabolic demands, allowing cells to better withstand cerebral ischemia. More specifically, the resulting decrease in the production of lactic acid and other acid metabolites tends to lessen secondary anoxic or vasogenic edema. The use of glycerol, naftidrofuryl and nimodopine to treat patients following acute ischemic stroke has also met with limited success.
A number of other therapeutic strategies for the treatment of stroke are under current investigation in the laboratory. One example is the proposed use of mild, whole-body hypothermia as a means of regulating the induction of heat shock proteins, which may play a role in protecting neural tissue from subsequent trauma in metabolic injury. Still another therapeutic approach involves the blockade of excitatory amino acid receptors which have been implicated in neuronal injury following prolonged anoxia. One such blocker is ketamine, dissociative general anesthetic. Other blockers include high concentrations of magnesium or antagonists of excitatory amino acids such kynurenate or aminophosphonovalerate. It will be appreciated by those skilled in the art that conventional stroke therapies are only marginally successful.
In recent years, multi-disciplinary investigations of physiological processes have provided evidence suggesting that electric and magnetic fields play an important role in cell and tissue behavior. In U.S. Pat. No. 4,818,697, entitled "Techniques for Enhancing the Permeability of Ions Through Membranes," which has been assigned to the assignee of the present invention and the disclosure of which is incorporated herein by reference, a method and apparatus are disclosed by which transmembrane movement of a preselected ion is magnetically regulated using a time-varying magnetic field. The fluctuating magnetic field is preferably tuned to the cyclotron resonance energy absorption frequency of the preselected ion. This important discovery brought to light the interplay of local magnetic fields and frequency dependence in ion transport mechanisms. It has now been discovered that by utilizing and extending the principles of cyclotron resonance tuning, unexpected and remarkable advances in the control and modification of physiological processes in living tissue can be achieved. In U.S. patent application Ser. No. 172,268, filed Mar. 23, 1988, the disclosure of which is incorporated herein by reference, the inventors of the present invention disclose that cyclotron resonance can be used to control tissue development. In U.S. patent application Ser. No. 254,438, entitled "Method and Apparatus for Controlling the Growth of Non-Osseous, Non-Cartilaginous, Solid Connective Tissue," filed Oct. 6, 1988, the disclosure of which is incorporated herein by reference, the present inventors disclose a method of controlling the growth of non-osseous, non-cartilaginous connective tissue which utilizes cyclotron resonance frequencies. In U.S. patent application Ser. No. 295,164, entitled "Techniques for Controlling Osteoporosis Using Non-Invasive Magnetic Fields," filed Jan. 9, 1989, the disclosure of which is incorporated herein by reference, the present inventors disclose a method of controlling osteoporosis using cyclotron resonance magnetic fields. In U.S. patent application Ser. No. 343,017, filed Apr. 25, 1989, entitled "Methods and Apparatus for Regulating Transmembrane Ion Movement Utilizing Selective Harmonic Frequencies and Simultaneous Multiple ion Regulation," the disclosure of which is incorporated herein by reference, the present inventors disclose a method of utilizing therapeutic higher-harmonic frequencies and a method of simultaneously controlling multiple ions. These various inventions deal with the transport of specific ions across cell membranes.
The present invention discloses a new and unique apparatus and non-invasive treatment therapy for stroke victims which is directed at relieving post-stroke difficulties that often lead to death or disability. This new treatment therapy may be used to supplement or replace conventional therapeutic modalities that employ a variety of pharmacologic agents.